This gene encodes a classical cadherin of the cadherin superfamily. Alternative splicing results in multiple transcript variants, at least one of which encodes a preproprotein that is proteolytically processed to generate the mature glycoprotein. This calcium-dependent cell-cell adhesion protein is comprised of five extracellular cadherin repeats, a transmembrane region and a highly conserved cytoplasmic tail. Mutations in this gene are correlated with gastric, breast, colorectal, thyroid and ovarian cancer. Loss of function of this gene is thought to contribute to cancer progression by increasing proliferation, invasion, and/or metastasis. The ectodomain of this protein mediates bacterial adhesion to mammalian cells and the cytoplasmic domain is required for internalization. This gene is present in a gene cluster with other members of the cadherin family on chromosome 16. [provided by RefSeq, Nov 2015]

TWIST2 regulates epithelial-mesenchymal transition by depriving the epithelial cell phenotype of E-cadherin and endowing the mesenchymal cell phenotype with Vimentin, which may be involved in the progression and prognosis of ovarian cancer.

Data show that grape seed proanthocyanidins could inhibit cell proliferation, invasion and migration of A549 cells, which might be related to the down-regulation of epidermal growth factor receptor and N-cadherin and the up-regulation of E-cadherin.

Evaluation of FoxC2 expression, alone or in combination with E-cadherin expression, may help to stratify non-small cell lung cancer patients for risk of disease progression, pointing to this EMT regulator as a potential prognostic marker

High E-cadherin concentration in presence of enhanced gamma-secretase activity is incontestably a paradoxically result, highlighting that E-cadherin loss is not a pre-requisite for Epithelial-Mesenchymal Transition.

The present study therefore indicated that IL-6 promoted the process of EMT in HIBECs as characterized by increased migration and invasion of HIBECs and the typical changes in mRNA and protein expression of the EMT markers E-cadherin and vimentin.

These data suggest that the number of polyploid giant cancer cells and the EMT-related proteins E-cadherin, N-cadherin, and vimentin may be valuable biomarkers to assess metastasis in patients with breast cancer.

MTA1 plays an important role in Epithelial-to-mesenchymal transition (EMT) to promote metastasis via suppressing E-cadherin expression, resulting in a poor prognosis in MPM. MTA1 is a novel biomarker and indicative of a poor prognosis in MPM patients

Data show that telomerase (hTERT) and ZEB1 protein form a complex, which directly binds to the E-cadherin promoter, and then inhibits E-cadherin expression and promotes epithelial-to-mesenchymal transition (EMT) in colorectal cancer cells.

CUGBP1 and HuR negate each other's effects in regulating E-cadherin translation by altering the recruitment of E-cadherin mRNA to PBs and play important roles in the regulation of intestinal barrier integrity.

Combined therapy with cytotoxic and anti-VEGF agents was shown to result in a significant increase in the number of cases of normal membrane localization of E-cadherin as compared with control (p = 0.00043) and cytotoxic therapy-alone (p = 0.01) groups

results indicate Moesin may regulate cell motility through its interactions with MT1-MMP and E-cadherin/p120-catenin adhesion complex and cytoplasmic expression of Moesin correlates with nodal metastasis and poor prognosis of OSCCs

ZIP5 knockdown inhibited the proliferation, migration and invasion of ESCC and suppressed COX2, cyclin D1 and E-cadherin expression, which led to the inhibition of cell progression in esophageal squamous cell carcinoma .

expression. E-cadherin may play a significant role in the sensitivity regulation of EGFR molecular targeting treatment. E-cadherin may provide important clues for selecting proper EGFR-TKI molecular targeting treatment

Demethylase recovered CDH1 gene expression may be involved in the apoptosis process. The beta-catenin protein translocated from the nucleus and cytoplasm to the membrane result in inactivation of b-catenin signaling pathway

All individuals with a CDH1 mutation had a personal or family history of diffuse gastric cancer. Patients with gastric cancer and germline CDH1 mutations had shorter survival times than patients who met the HDGC criteria but did not have CDH1 mutations.

knockdown of ILK inhibits glioma cell migration, invasion and proliferation through upregulation of E-cadherin and downregulation of cyclin D1. Our results suggest that ILK may serve as a promising therapeutic target for glioma.

Cyclin B1 could suppress the invasion and metastasis of colorectal cancer cells through regulating E-cadherin expression, which enables the development of potential intervention strategies for colorectal cancer.

We demonstrate the potential of common inherited genetic variants to inform patient outcome and show that cdh1's rs9929218 identifies approximately 8% of colorectal cancer patients with poor prognosis.

The results from the current study indicate that the hypermethylation frequency of E-cadherin in NSCLC is strongly associated withnon-small cell lung carcinoma incidence and it may be an early event in carcinogenesis

CDH1 germline variants are present in early-onset diffuse gastric cancer patients in Chinese population, but they are mainly missense variants with unknown function which are likely associated with lymph node metastasis and survival.

The aim of this study was to investigate immunohistochemically the E-cadherin/N-cadherin "switch" and vimentin expression as markers of epithelial-mesenchymal transition process in tongue oral squamous cell carcinomas.

Exogenous expression of cell surface E-cadherin converts statin- sensitive cells to a partially resistant state implying that statin resistance is in part dependent on the tumor cells attaining an epithelial phenotype

Observed strong association of promoter hypermethylation of CDH1 with Gastric cancer(OR = 12.23) suggesting that epigenetic regulation of CDH1 could play a critical role in the etiology of Gastric cancer.

CCND1 870G/A and CDH1 -160C/A SNPs may contribute to the etiology of colorectal cancer in South Indian population and carriers of the 870A/-160A haplotype have a higher risk for colorectal cancer susceptibility.

Results showed that E-cadherin loss disrupts the organization of the cell's actin and microtubule cytoskeletons and modifies its adherence and migration characteristics but is insufficient to induce an epithelial to mesenchymal transition.

The loss of membranous E-cadherin with increase in cytoplasmic accumulation in differentiative layers of epithelium through the progression of dysplasia was noted along with up-regulation in VEGF expressions

CD133 associates with beta-catenin in early placodes, and its continued expression correlates with loss of beta-catenin and E-cadherin from the cell membrane at a time when E-cadherin transcriptional repressors Snail and Slug are not implicated.

MMP-2, MMP-9, and E-cadherin are expressed in the endometrium of infertile patients during the receptive phase of the natural menstrual cycle. However, there is no correlation between the expression of these molecules and the clinical IVF outcomes.

In pancreatic adenocarcinoma cells, PAR3 knockdown enhances cell adhesion. We propose this is due to increased expression of E-cadherin, leading to a greater adhesion of free-floating cells to cells bound to the surface via integrins, particularly ITGalphav.

The expression of PRL-3, but not of E-cadherin, was associated with shorter survival of patients. PRL-3 and E-cadherin exhibit interactions in gastric cancer and are involved in the formation of lymph node metastases.

highly sensitive rabbit E-cadherin antibody is the preferred antibody for evaluating ductal carcinomas and for distinguishing ductal versus lobular lesions, and the dual stain was superior to the single E-cadherin stain

Two novel CDH1 mutations were found. The c.602_603delCT mutation results in a frame-shift and a premature stop at codon 207, and is classified as pathogenic. The functional consequence of the c.1565 + 3insTT mutation was unknown and not as obvious.

We have shown that germline CDH1 mutations are associated with early onset of bilateral lobular carcinoma in situ with or without Invasive lobular breast cancer in women without a family history of gastric cancer.

A more complete study of the prognostic and predictive role of E-cadherin expression in patients with Stage I-II NSCLC will help identify a prognostically unfavorable group of patients who may be given additional treatment in the postoperative period.

E-cadherin protein expression in the cecum was lower in IBS-A compared with controls and associated with longstanding symptoms. E-cadherin was further associated with abdominal pain severity in the IBS group overall, but unrelated to IBS subtype.

These results indicated a possible effect of SIRT1 and p300/CBP involved in regulating the expression of E-cadherin and MLH1, thus participating in the tumor progression of gastroesophageal junction cancer

Data show that miR-148a downregulated vimentin expression and upregulated E-cadherin expression, suggesting that miR-148a inhibited epithelial-mesenchymal transition (EMT), and the SMAD2 gene was identified as the direct and functional target of miR-148a.

The expression of E-cadherin and beta-catenin, combined with cytological and architectural analysis, may highlight different immunophenotypes and improve classification of breast carcinomas in situ with mixed pattern.

this study shows that sEcad is a novel candidate protein for drug targeting since it is increased in human and mouse HER2-positive (HER2+) breast tumors, MMTV-PyMT bodily fluids and human cell culture systems.

These findings support the potential value of E-cadherin for a supplementary differentiation of molecular subtypes of breast carcinoma, based on the biological significance of its capacity of expression.

Suggest that ZEB1 overexpression, associated with E-cadherin and miR-200s downregulation, and the expression of mesenchymal markers might enhance the metastatic potential of undifferentiated endometrial carcinomas.

Data indicate that pancreatic (pro)enzymes enhanced expression of beta-catenin and E-cadherin and decreased expression of several epithelial-mesenchymal transition (EMT)-associated genes, such as Vimentin, Snail and Slug.

results suggest that reduced expression of E-cadherin is associated with promoter methylation of E-cadherin gene, in addition to providing evidence for the aberrant nuclear localization of E-cadherin in epithelial ovarian carcinoma

alterations of their expression suggest a role of Dsg3 and gamma-catenin (additionally to E-cadherin/beta-catenin) as biomarkers of malignant transformation risk of oral dysplasia and the biological behavior (aggressiveness) of oral cancer, respectively

Overexpression of delta-catenin reduces the expression of E-cadherin and alters the balance between E-cadherin and p120ctn, which in turn affects the formation of intercellular adhesions and promotes invasion and metastasis in colorectal cancer.

In oral squamous cell carcinoma the probability to have or develop metastases was very low when high E-cadherin expression was found in a preoperative sample or when a low podoplanin expression was found

LSD1 expression was higher, while E-cadherin expression was lower, in colon cancer specimens of high TNM stage and with distant metastasis. Positive LSD1 expression and negative E-cadherin expression were correlated with lower overall survival.

Data confirm that E-cadherin and COX-2 expressions are related to OSF. The epigenetic changes presented in patients with chronic inflammation might demonstrate an irreversible destruction in the tissues or organs similar to the effects of cancer.

The data showed that both fascin and vimentin proteins were significantly overexpressed in cholangiocarcinoma, whereas E-cadherin expression was reduced in cholangiocarcinoma compared with normal tissues.

CDH1 missense mutations were found in 4 out of 81 (5%) patients with non-syndromic OFC. This finding opens a new pathway to reveal the molecular basis of non-syndromic OFC. Cancer risk among carriers of these mutations needs to be defined.

Results show a role for E- and P-cadherin co-expression in breast cancer progression and highlight the potential benefit of targeting P-cadherin in the aggressive tumours expressing high levels of this protein.

After exposure to hypoxia, HIF-1alpha protein was up-regulated, both mRNA and protein levels of E-cadherin were down-regulated and MMP-2 was up-regulated, while HIF-1alpha mRNA showed no significant change

Loss of SARI expression initiates epithelial-to-mesenchymal transition (EMT), which is visualized by repression of E-cadherin and up-regulation of vimentin in lung adenocarcinoma cell lines and in clinical lung adenocarcinoma specimens.

We conclude that determination of E-cadherin expression can be used as an adjunct in selecting patients who may benefit from adjuvant chemotherapy in the presence of otherwise favorable prognostic factors.

These results provide strong evidence that the methylation status of E-cadherin gene contributes to a reduction in the expression of E-cadherin mRNA, and may play a role in the development and progression of non-small cell lung cancer.

A meta-analysis indicated that the -160A allele of E-cadherin provides a higher risk for the development of prostate and urothelial cancers and a protective role for colorectal cancer in an ethnicity-dependent manner.

The expressions of E-cd and alpha-cat are significantly lower in prostate cancer than in benign prostatic hyperplasia, and they are not associated with cancerous metastasis, but negatively correlated with the PSA level in PCa patients.

findings show that alpha-catulin is highly expressed in melanoma cells; expression of alpha-catulin promoted melanoma progression and occurred concomitantly with the downregulation of E-cadherin and the upregulation of expression of mesenchymal genes

these results demonstrate a Fyn kinase-dependent mechanism through which IFNgamma regulates E-cadherin stability and suggest a novel mechanism of disruption of epithelial cell contact, which could contribute to perturbed epithelial barrier function.

Investigated the expression of RKIP and E-cadherin in lung squamous cell carcinoma tissue. The rates of positive RKIP and E-cadherin mRNA expression were significantly lower in lung squamous cell carcinoma than in the surrounding normal tissues.

Data show that Acinetobacter baumannii transposase Tnp in A549 cells induced DNA methylation of CpG regions in the promoters of E-cadherin (CDH1) gene, whereas the cytoplasmic localization of the truncated Tnp without NLSs did not induce DNA methylation.

This calpain-mediated proteolysis of E-cad generates the formation of the lymphovascular embolus and is responsible for its unique properties of increased homotypic adhesion, apoptosis resistance and budding.

our results indicated that plasma CDH1 levels may serve as a risk marker against gastric cancer and variant genotypes of rs26160 and rs17690554 may contribute to the etiology of diffuse gastric cancer in this study.

Although the expressions of E-cadherin and N-cadherin appear to be correlated with survival outcomes in bladder cancer, N-E cadherin switch may be a better predicator for postoperative recurrence and cancer-related survival.

Results show that the adipocytokines and glucocorticoid metabolism-related genes are overexpressed in colorectal adenocarcinomas, and expression of these genes is associated with the downregulation of E-cadherin mRNA.

E-cadherin expression was present in 100% of cases of both adenocarcinomas and adenomas, with prevailing strong membranous immunoreactivity and no differences between protein expression in tumors and normal mucosa.

The modifications of E-cadherin by O-GlcNAcylation and lack of pro-region processing represent novel mechanisms for rapid regulation of cell surface transport of E-cadherin in response to intoxication.

CDH1 polymorphisms can contribute to the etiology of premalignant skin lesions in people chronically exposed to arsenic in drinking water, and that this gene may be a factor in individual susceptibility to cutaneous diseases.

E-cadherin inhibits nuclear accumulation of Nrf2 and Nrf2-mediated gene transcription by its interaction with Nrf2; findings imply that chemoresistance of cancer cells upon the loss of E-cadherin might be associated with Nrf2

Hakai dimerization allows the formation of a phosphotyrosine-binding pocket that recognizes specific phosphorylated tyrosines and flanking acidic amino acids of Src substrates, such as E-cadherin, cortactin and DOK1.

E-cadherin is extensively expressed by oropharyngeal squamous cell carcinoma, even the non-keratinizing type, but our results suggest that cadherin expression may not be a predictor for nodal or distant metastasis in these tumors.

Study concludes that Smad3 regulates, at the transcriptional level, miR-200 family members, which themselves regulate ZEB1 and ZEB2, known transcriptional repressors of E-cadherin, at the posttranscriptional level in a TGF-beta-independent manner.

there are correlations between beta-catenin and TNM stage of colorectal cancer; there are greater amounts of beta-catenin in patients with deeper invasion of the tumor in colon layers, lymph node involvement as well as in patients with distant metastasis

study presents evidence that in the cadherin-catenin complex alpha-catenin contributes to the binding strength of another catenin, p120, to the same complex; data suggest that alpha-catenin-p120 contact within the cadherin-catenin complex can regulate cadherin trafficking

Data suggest that the TBX2/NRAGE complex protects cells against anoikis by downregulating p14ARF, representing a novel pathway for the regulation of anoikis by epithelial-to-mesenchymal transition and E-cadherin.

Results sugggest that histone deacetylation of E-cadherin (CDH1) and downregulation of miR-373, together with the hypermethylation of CDH1 by hepatitis B virus-encoded X antigen, HBx, may be important for the understanding of HBV-related carcinogenesis.

elevation of E-cadherin, a cell adhesion molecule and suppression of beta-catenin, a proto-oncogene have been observed in presence of CaSR agonists whereas reverse effect has been seen in presence of CaSR antagonist

these findings show that epithelial-mesenchymal transition and its down-regulated expression of E-cad circumvent breast cancer dormancy in part by facilitating beta1 integrin expression necessary for metastatic outgrowth.

The deubiquitinase USP37 binds CDH1 and removes degradative polyubiquitin from cyclin A. USP37 was induced by E2F factors in G1, peaked at G1/S, and was degraded in late mitosis. Phosphorylation of USP37 by CDK2 stimulated its full activity.

These findings show an important role for p53 in the progression of serous borderline ovarian tumors to an invasive carcinoma, and suggest that downregulation of E-cadherin by DNMT1-mediated promoter methylation contributes to this process.

in patients with gastric caancer, expression of E-cadherin and that of Slug were associated with tumor properties, including lymph node metastasis, stage, lymphatic invasion, and venous invasion, as well as with prognosis

GLI1-upregulated MUC5AC interfered with the membrane localization of E-cadherin, leading to decreased E-cadherin-dependent cell-cell adhesion and promoting the migration and invasion of pancreatic ductal adenocarcinoma cells.

findings show that p53 has an important role in the progression from serous borderline ovarian tumors to invasive carcinomas. In addition, our findings suggest that downregulation of E-cadherin by the PI3K/Akt pathway contributes to this progression

ECAD inhibits Smad3/2 phosphorylation by recruiting RhoA to p120-ctn at the p120-ctn binding domain, whereas the loss of ECAD due to cadherin switching promotes the up-regulation of TGFbeta1 and its target genes, and facilitates liver fibrosis.

These results provide evidence that E-cadherin is expressed in a proportion of invasive lobular carcinoma of the breast, however, unlike ductal carcinoma, its expression seems to be of limited significance.

A negative correlation is found between Ezrin and E-cadherin expression in nasopharyngeal carcinoma tissues. Ezrin and E-cadherin are closely related to clinical staging and cervical lymph node metastases.

Suggest that TC21 promotes cell motility and metastasis by regulating the expression of E-cadherin and N-cadherin in hepatocellular carcinoma and is associated with tumor progression and poor prognosis in HCC.

In lung carcinomas dysadherin expression seems to reflect tumour aggressiveness and may be considered a positive marker of poor prognosis when considered alone or/and in combination with down-regulation of E-cadherin.

Inactivation and disassembly of the anaphase-promoting complex during human cytomegalovirus infection is associated with degradation of the APC5 and APC4 subunits and does not require UL97-mediated phosphorylation of Cdh1.

the motility of E-cadherin within, and away from, the cell surface are not exclusive or independent mechanisms and there is a fine balance between the two which when perturbed can have dramatic effects on the regulation of Adherens Junctions

in the 123 TNBC cases, the prognosis of patients with an E-cadherin-negative expression was significantly worse than that of E-cadherin-positive patients (P=0.0265), especially for those in clinical stage II (P=0.002).

The study objective was to assess changes in the expressions of E-cadherin and alpha-, beta- and gamma-catenin proteins in pancreatic duct carcinoma in correlation with clinicopathological parameters, lymph node involvement and distant metastases.

Results suggest that CDH1 gene methylation and H pylori infection are frequent events in samples from Brazilian patients with chronic gastritis and reinforces the correlation between H. pylori infection and CDH1 inactivation in early gastric tumorigenesis

impaired down-regulation of E-cadherin and beta-catenin, along with Wnt/beta-catenin signaling pathway activation during the window of implantation, might be one of the potential molecular mechanisms of infertility in patients with endometriosis.

Loss of E-cadherin expression was high in gallbladder cancer(67%), while majority of the chronic cholecystitis (94%) and xanthogranulomatous cholecystitis (91%) cases retained positive E-cadherin expression.

miR-9 miRNA downregulates E-cadherin. Expression of miR-9 is activated by MYC and MYCN, which bind to the mir-9-3 locus. Elevated expression of miR-9 may contribute to epithelial-mesenchymal transition and metastasis in some and possibly many tumours.

L1 binding to ankyrin alters the regulation of neuronal branching and leads to a decrease in perisomatic synapses of GABAergic inhibitory interneurons in the developing transgenic mouse cingulate cortex.

Results indicate that cells underwent EMT exhibited overactive TGFbeta signaling and loss of expression of the CDH1, CGN, CLDN4, and KLK10 genes as a result of hypermethylation of their corresponding promoter regions.

The results indicate that developmentof an invasive carcinoma from an intraductal papillary mucinous neoplasms of pancreas (IPMN) is associated with a decrease in tumor cells expressing E-cadherin and beta-catenin and higher proliferative activity.

molecular pathway from hypoxia to cellular transformation includes up-regulation of HIF and subsequent transcriptional induction of LOX and LOXL2, which repress E-cadherin and induce epithelial to mesenchymal transition

Either overexpression of a key regulator of cell cycle, Mad2, or knock down of Aurora B, an important kinase in mitosis, or Cdh1, a key E3 ligase in cell cycle, resulted in a significant increase of SP cells in CNE-2.

IBH-6 and IBH-4 breast cancer cells show down-regulation of E-cadherin expression with aberrant protein localization, and up-regulation of Twist; these features can be related to their invasive/metastatic characteristics.

The combination of the upregulation of vimentin and aberrant expression of E-cadherin/beta-catenin complexes at the tumour invasive front may provide a useful prognostic marker in oral squamous cell carcinoma.

Data show that P-cadherin overexpression in breast cancer cells with wild-type E-cadherin promotes cell invasion, motility, and induces the secretion of MMP-1 and MMP-2, which then lead to P-cadherin ectodomain cleavage.

Data show that conversion of Ras-expressing keratinocytes from a premalignant to malignant state induced by decreasing E-cadherin function was associated with and required an approximately two to threefold decrease in RalA expression.

pH 6.6 activates Src kinases, resulting in tyrosine phosphorylation of E-cadherin and p120ctn and a weakening of the association of E-cadherin with p120ctn and contributing to the instability of E-cadherin at adherens junctions

the ability of CBX7 to positively regulate E-cadherin expression by interacting with HDAC2 and inhibiting its activity on the E-cadherin promoter would account for the correlation between the loss of CBX7 expression and a highly malignant phenotype

The main objectives were to assess tumor proliferation and invasiveness biomarkers (Ki-67, E-cadherin) and to identify potential correlation between biomarkers and classic prognostic factors in cervical cancer.

Investigated methylation status of the CDH1 promoter in gastric cancer patients. A difference was found between the methylation level of the two alleles in some samples, but there was no mono-allelic promoter hypermethylation in any of the samples.

Data suggest that cadherin dimerization proceeds via an induced fit mechanism where the monomers first form a tryptophan-2 independent initial encounter complex and then undergo subsequent conformational changes to form the final strand-swapped dimer.

Data suggest that E-cadherin-based cell-cell adhesion limits Wnt signals by promoting the activity of a junction-localized beta-catenin phosphodestruction complex, which may be relevant to tissue morphogenesis and cell fate decisions during development.

E-cadherin may coengage KLRG1 and alpha(E)beta(7) and that KLRG1 overcomes its exceptionally weak affinity for cadherins through multipoint attachment to target cells, resulting in inhibitory signaling.

Data indicate CDH1-160C>A is a risk factor for CRC, and because a high proportion of the European population are carriers of at-risk genotypes, the variant is likely to contribute substantially to the development of colorectal cancer (CRC).

Studies show for the first time that DPAGT1 is an upstream regulator of E-cadherin N-glycosylation status and adherens junction composition and suggest that dysregulation of DPAGT1 causes disturbances in intercellular adhesion in oral cancer.

decreased expression of E-cadherin in upper urothelial carcinoma (UUC) in regions affected by Balkan Endemic Nephropathy tumors may be linked to tumor growth, while expression of E-cadherin in control tumors may be associated with tumor grade.

alpha(2)-, alpha(3)-, and beta(1)-integrins and E-cadherin expression in normal human lung and bronchopulmonary sequestration and congenital cystic adenomatoid malformation were evaluated using Western blot and immunohistochemistry.

results demonstrate an association between polymorphisms within the CDH1 (E-cadherin) gene and Crohn's disease, which leads to cytoplasmic accumulation of E-cadherin instead of its normal localisation at the plasma membrane/adherens junction.

N- and E-cadherin expression in the human fetal ovary indicates likely roles in gonadal development from germ cell proliferation to primordial follicle formation, as well as in the development of the urogenital ducts of both genders.

p190RhoGAP and p120ctn associated predominantly on the plasma membrane of cells overexpressing E-cadherin, and that E-cadherin-bound p120ctn contributed to RhoA inactivation by favoring p190RhoGAP-RhoA association.

Ras transformation has at least two independent actions to disrupt E-cadherin junctions, with effects to cause both mislocalization of E-cadherin away from the cell surface and profound decrease in the expression of E-cadherin

The resistance of E-cadherin over-expressing cells to staurosporine may due to the up-regulation of Bcl-2/Bax ratio. When E-cadherin interference plasmids were transfected into MCF-7 cells, Bcl-2 expression was down-regulated.

In hepatocellular carcinoma (HCC), there is a negative correlation between the positive expression of p130Cas and the normal expression of E-cadherin/beta-catenin. p130Cas plays important roles in the invasion, metastasis and prognosis of HCC.

Tbx2 and Tbx3 may play a dual role during the radial to vertical growth phase transition by both inhibiting senescence via repression of p21(CIP1) expression, and enhancing melanoma invasiveness by decreasing E-cadherin levels.

The -347del allele of E-cadherin strongly links with the +178T and +234 13N ins alleles. The -347del/del genotype may increase susceptibility of sporadic gastric carcinoma among males in high-risk areas of China.

significant association of concurrent expression of unmethylated E-cadherin gene and E-cadherin protein with metastatic prostate cancer cells in bone. May have role in intercellular adhesion in formation of metastatic lesions in bone.

In the gastric cancerous tissues, the expression percentage of Wnt-1, beta-catenin and E-cadherin is 54.4%, 45.6%, 47.2%, respectively, which is significantly higher than the percentage expression of these genes in normal tissues (p<0.01).

Sequence analysis of the high-frequency region along E-cadherin exons 7-9 revealed a number of sequence alterations in the patient group as a whole. A C insertion at nt 76,598 was found in 2 African American patients.

Results show that InlA triggers two successive E-cadherin post-translational modifications, the Src-mediated tyrosine phosphorylation of E-cadherin followed by its ubiquitination by the ubiquitin-ligase Hakai.

The Matrix Metalloproteinase (MMP-2, MMP-9) to E-cadherin (M/E ratio) characterizes an important aspect of the molecular phenotype associated with the histologic progression of prostate cancer among African American prostate cancer patients.

Results suggest that a decrease in E-cadherin gene expression level in high-grade neuroepithelial tumors may be a hallmark of malignancy in dedifferentiated tumors and that it may be possibly correlated with their progression and dissemination.

loss of E-cadherin is probably consequent on p120 loss or decrease. Aberrations and other alterations of the E-cadherin gene are unlikely to be responsible for the loss of E-cadherin in solid pseudopapillary tumors.

Rsults suggest that the lower epithelial alpha-catenin, E-cadherin and (or) ZO-1 expression in patients with atopic asthma contributes to a defective airway epithelial barrier and a higher influx of eosinophils in the epithelium.

loss of expression of the miR-200 family members may play a critical role in the repression of E-cadherin by ZEB1 and ZEB2 during EMT, thereby enhancing migration and invasion during cancer progression.

study of correlation between mutations & expression of E-cadherin, beta-catenin, occludin & claudin & complexity of colon carcinoma growth; perturbed expression & distribution of these proteins was found, but could not be linked to complexity of growth

Data show that the haplotype the E-cadherin gene may have impact on the risk of epithelial ovarian carcinoma. The CC genotype of 3'-UTR + 54CT may be a potential risk factor for the epithelial ovarian carcinoma.

This study provides into the mechanisms underlying the functional role of EZH2 overexpression in gastric cancer cells and a new modality of regulation of E-cadherin expression in silencing mechanisms of tumor suppressor genes.

No CDH1 polymorphisms or haplotypes were associated with GC risk, no differences of effect were seen by H pylori infection. Three CDH1 polymorphisms in the same haplotype interacted with smoking to increase GC risk in smokers but not in never smokers.

ASH1 inactivates DKK1 and DKK3, negative regulators of Wnt/beta-catenin signaling, E-cadherin, and integrin beta1 through ASH1-mediated deacetylation and repressive trimethylation of lysine 27 of histone H3 in the promoter regions of DKK1 and E-cadherin.

PTPRK influences transactivating activity of beta-catenin in non-tumoral and neoplastic cells by regulating the balance between signaling and adhesive beta-catenin, thus providing biochemical basis for the hypothesis of PTPRK as a tumor suppressor gene.

study describes activation of EGFR by mutant E-cadherin as a novel mechanism in tumor cells that explains the enhanced motility of tumor cells in the presence of an extracellular mutation of E-cadherin

Noncohesive pancreatic cancers were characterized by the loss of E-cadherin protein expression. Promoter hypermethylation is a possible mechanism of E-cadherin gene silencing in a subset of these cancers.

the CaR regulates cell survival and Ca(2+)(o)-induced differentiation in keratinocytes at least in part by activating the E-cadherin/PI3K pathway through a Src family tyrosine kinase-mediated signaling

In most hereditary cancer syndromes, like hereditory diffuse gastric cancer and lobular carcinoma of the breast, multiple organ sites are affected by cancer and have been shown to be associated with germline mutations in CDH1 at 16q22.1.

The C/C genotype of 3'-UTR C/T SNP and -160C/-374GA haplotype in E-cadherin gene may be a factor for risk of epithelial ovarian cancer in Chinese; the lower expression of E-cadherin might play a role in the pathogenesis of epithelial ovarian cancer.

membranous overexpression of E-cadherin and beta-catenin are associated with the metastatic prostate cancer cells in bone and the high frequency of expression suggests their involvement in the intercellular adhesion of the metastatic cells in bone

Somatic E-cadherin mutations affect apoptosis regulation in that way that they can facilitate the disruption of adherens junctions thereby possibly influencing the response to cisplatin-based chemotherapy.

Our results suggest that methylation of E-cadherin is a frequent, early event in gastric carcinoma progression. Two factors were ...associated with lymph node metastasis: abnormal expression of E-cadherin and lymphatic invasion

Our findings suggest that the hypermethylation of E-cadherin promoter might be involved in the process of gastric carcinoma through the specialized factors in H. pylori-induced enlarged fold gastritis.

Analysis of interface of In1a protein with E-cadherin to identify single amino acid substitutions in InlA that would potentially improve the overall quality of interaction and hence increase the weak binding affinity of the complex

The E-cadherin gene methylation presence in tumors with lowest invasive and metastatic potential suggests the early involvement of this epigenetic event in the multistep progression of the oral carcinogenesis

A novel germline CDH1 truncating mutation in the extracellular portion of the protein (517insA) was found in 2 relatives with lobular breast cancer. Germline CDH1 mutations can be associated with invasive LBC in the absence of diffuse gastric cancer.

The major subtypes of renal epithelial neoplasms display differential aberrant CDH1, PTGS2, and RASSF1A promoter methylation levels. This gene panel might contribute to a more accurate discrimination among common renal tumors.

In addition to suppressing late-stage tumor progression, E-cadherin-mediated adherens junctions may also contribute to the initial emergence of a cohesive morphogenic phenotype that is a hallmark of differentiated epithelial ovarian carcinoma.

we explored the implication of three proteins (E-cadherin, a- and b-catenins) that form the cadherin-catenin complex, a receptorial structure strictly involved in tumoral vascular invasion and embolization in this biologic event

E-cadherin signaling is an important activator of c-Src at cell-cell contacts, providing a key input into a signaling pathway where quantitative changes in signal strength may result in qualitative differences in functional outcome.

Recurrent CDH1 mutations in families with hereditary diffuse gastric cancer are due to both independent mutational events and common ancestry. The presence of a founder mutation from Newfoundland is strongly supported.

CDHE was expressed in both tumor types, especially in the cytoplasm and cell membrane of the cuboidal cells and to a lesser extent in the polygonal cell membrane, where it was expressed mostly in the cytoplasm.

E-cad expression to be correlated with E-cad methylation at highly statistically significant levels. Above a threshold of approximately 20% to 30% mean methylation, the expression of E-cad was effectively silenced.

the recruitment of PI3K to the E-cadherin/beta-catenin/p120-catenin complex via beta-catenin at the plasma membrane is required for calcium-induced phospholipase C-gamma1 activation and, ultimately, keratinocyte differentiation

targeting constitutive expression of AP-2alpha in AP-2-positive KM12C colon cancer cells with small interfering RNA resulted in an increase in their invasive potential, downregulation of E-cadherin and increased expression of MMP-9

In conclusion, ROS play a central role in mediating TPA-triggered sustained PKC and ERK signaling for regulation of gene expression of integrins and E-cahedrin that are responsible for EMT and migration of HepG2.

loss of extracellular E-cadherin observed in normal duodenal & colonic mucosa in patients familial adenomatous polyposis might play a role in high susceptibility of these tissues for (pre-) malignant transformation

Our results indicate a functional role of Met-E-cadherin interaction in MCF-7 cells through the amplification of the signaling downstream of HGF-Met triggering that involved c-Src and phosphoinositide-3-kinase activities.

The high frequency of methylation of the CDH1 gene promoter suggests that the inactivation of tumor suppressor genes and of the genes related to the control of cellular proliferation through this mechanism is involved in gallbladder carcinogenesis.

Findings demonstrate a stimulatory role for E-cadherin in proliferative regulation, and identify a simple mechanism by which cell-cell contact may trigger or inhibit epithelial cell proliferation in different settings.

Our present results show that gastric differentiated-type carcinomas have different characteristics according to the phenotypic marker expression of the tumour in terms of histological findings, E-cadherin expression and pattern of chromosomal changes.

These results suggest that Scrib stabilizes the coupling between E-cadherin and the catenins and are consistent with the idea that mammalian Scrib could behave as a tumor suppressor by regulating epithelial cell adhesion and migration.

CDH-1 is closely related to metalloproteinase and plays important but not well-understood role in onset and progression of primary open angle glaucoma. Role could be resolved by posttranslated products of gene and protein-protein interaction.

With tumor progression and development of heterogeneity, the abnormal expressions of MMP-9, TIMP-2, and E-cadherin or DNA aneuploid rate or high SPF gradually increases, suggesting that they play a crucial role in gastric carcinoma progression

The TGFbeta(1)-induced destabilisation of E-cadherin-mediated cell-cell adhesion involves phosphorylation of beta-catenin, which is regulated by E-cadherin adhesion complex-associated PI3-kinase and PTEN.

upon infection of quiescent cells human cytomegalovirus not only activates the E2F-dependent G(1)/S transcription program but also facilitates protein accumulation of APC/C substrates by rapid Cdh1 dissociation

cadherin switching (downregulation of E-cadherin and upregulation of N-cadherin) is necessary for increased motility but is not required for the morphological changes that accompany the epithelium-to-mesenchyme transition

All 61 meningothelial meningiomas, 10 of 12 invasive meningiomas, and 3 of 5 anaplastic meningiomas were positive for both ECAD and beta-catenin, while these were both negative in all of the fibrous meningiomas.

Review summarizes divergent studies that provide evidence of the function of E-cadherin trafficking and the puzzle of how this adhesion molecule is regulated and managed throughout the life of the epithelial cell.

Cdx1 or Cdx2 expression is sufficient to induce E-cadherin-dependent adhesion of COLO 205 cells associated with polarization and cell-cell membrane compaction, as well as induction of differentiated gene-expression pattern.

E-cadherin and epidermal growth factor receptor (EGFR) are associated in mammary epithelial cells and that E-cadherin engagement in these cells induces transient activation of EGFR, as previously seen in keratinocytes.

We conclude, therefore, that two major components of cell-cell interaction synergistically regulate cell cycle progression in HEK293 cells by regulating p21 expression in a beta-catenin/TCF-dependent manner.

A recombinant E-cadherin lacking free sulfhydryl groups and its mutants with novel cysteines were expressed. The coexistence of the structurally identical adhesive and lateral dimers suggests some flexibility of the extracellular cadherin region.

provides support that E-cadherin induction by WNT/beta-catenin signaling is an evolutionarily conserved pathway operative in lung cancer cells and that loss of expression may be important in lung cancer development or progression

Data demonstrate a direct role of E-cadherin/catenin complex organization in the regulation of matrix metalloproteinases and suggest an implication of this regulation in the expression of an invasive phenotype by bronchial tumor cells.

The molecular requirements for E-cadherin to activate Rac signaling thus appear distinct from those that stimulate PI3-kinase, and we postulate that p120-ctn may play a central role in the E-cadherin-Rac signaling pathway.

Pulse-labeled beta-catenin replaces the beta-catenin bound to the cell surface prebiotinylated E-cadherin immediately after synthesis or arrives at the plasma membrane in a complex with the E-cadherin precursor.

matrix metalloproteinase-2 and 9 and membrane-type 1 matrix metalloproteinase mRNA expression in endometriosis was higher than in normal endometrium whereas E-cadherin, alpha- and beta-catenin mRNA expression was not suppressed in endometriosis

The presence of E-cadherin mutations can significantly alter the accumulation of the apoptosis-regulating p53 protein, whereas no correlation with the p53 mutation status or with Ki-67 staining was observed.

Loss of E-cadherin expression followed by expression of the mts1 gene may be an important event for increasing cell proliferation, motility and invasion activity in the progression of gallbladder cancer.

The reduction of E-cadherin and beta-catenin expression was related to invasiveness and proliferative status of prolactinomas and correlated with the more aggressive behavior of prolactinomas in men compared with in women.

results indicate that expression of E-cadherin in IST-1 trophoblast cells results in a contact-mediated inhibition of motility and invasion and suggest an important role for E-cadherin down-regulation in the intermediate trophoblast during implantation

results suggest that the inadequate trophoblastic invasion, induced by antiphospholipid antibodies, can be the result of decreased alpha1 integrin and VE-cadherin and increased alpha5 integrin and E-cadherin expression in the trophoblast